‘HOSPITAL CASE STUDY’

Introduction:
Cirrhosis is scarring (fibrosis) of the liver caused by long-term liver damage. The scar tissue prevents the liver
working properly. Cirrhosis is sometimes called end-stage liver disease because it happens after other stages of
damage from conditions that affect the liver, such as hepatitis.

Types of liver cirrhosis

Alpha-1 antitrypsin deficiency (build-up of an abnormal protein in the liver) Hemochromatosis (excess iron stored
in the liver). Wilson disease (excess copper stored in the liver). Cystic fibrosis (sticky, thick mucus builds up in
the liver).

Causes cirrhosis of the liver

Cirrhosis is a type of liver damage where healthy cells are replaced by scar tissue. Common causes include
excessive drinking of alcohol, hepatitis B and C virus infections, and fatty liver that's caused by obesity and
diabetes.

Complications of cirrhosis
Major complications of cirrhosis include ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, portal
hypertension, variceal bleeding, and hepatorenal syndrome.

Stages of Cirrhosis
• There are 2 stages of cirrhosis: compensated cirrhosis and decompensated cirrhosis (clinical stages)
• The stages are dynamic and progressive, but there is potential reversibility from the decompensated to
compensated stage.
• Compensated cirrhosis is the asymptomatic stage
Epidemiology

Cirrhosis is a leading cause of mortality and morbidity across the world. It is the 11th leading cause of death and
15th leading cause of morbidity, accounting for 2.2% of deaths and 1.5% of disability-adjusted life years
worldwide in 2016. CLD caused 1.32 million deaths in 2017, approximately two-thirds among men and one-third
among women.

Historically, viral hepatitis has been the leading etiology for CLD. However, improved prevention strategies (in
the case of hepatitis B) and treatment (in the case of hepatitis C) have led to improving CLD trends. This is reflected
in global declines that have been observed in liver disease mortality rates over the past 30 years. Specifically, the
age-adjusted death rate (AADR) from CLD has declined from 21 to 16.5 per 100,000 population from 1990 to
2017. As depicted in these declines have been most marked for liver disease from hepatitis B infection.

Meanwhile, obesity and alcohol consumption, which are common and increasing in many parts of the world, have
become key liver disease risk factors. They are anticipated to drive CLD epidemiology going forward and to
account for increasing proportions of death in the future, although mortality trends have not yet reflected their
impact
Etiology

The most common causes of cirrhosis of the liver are: Alcohol abuse (alcohol-related liver disease caused by long-
term [chronic] use of alcohol). Chronic viral infections of the liver (hepatitis B and hepatitis C). Fatty liver
associated with obesity and diabetes and not alcohol.

Pathophysiology
Liver cirrhosis is the final common pathological pathway of liver damage arising from a wide variety of chronic
liver diseases. The etiology of cirrhosis varies geographically, with alcoholism, chronic hepatitis C virus infection,
and nonalcoholic fatty lives disease (NAFLD) being the most common causes in western countries, whereas
chronic hepatitis B is the primary cause of liver cirrhosis in the Asia-Pacific region. Liver cirrhosis has many other
causes, include inherited diseases such as hemochromatosis and Wilson’s disease, primary biliary cirrhosis,
primary sclerosing cholangitis, and autoimmune hepatitis. Some cases are idiopathic or cryptogenic. In recent
decades, NAFLD has become a leading cause of chronic liver disease in Western countries such as the United
States, with a prevalence of as high as 30% in the general population. Thus, NAFLD has attracted extensive
attention as an important cause of chronic liver diseases.

Although the causes of liver cirrhosis are multifactorial, there are some pathological characteristics that are
common to all cases of liver cirrhosis, including degeneration and necrosis of hepatocytes, and replacement of
liver parenchyma by fibrotic tissues and regenerative nodules, and loss of liver function
Sign and symptoms

• yellowing of the skin and whites of the eyes (jaundice)

• vomiting blood.
• itchy skin.
• dark pee and tarry-looking poo.
• bleeding or bruising easily.
• swollen legs (oedema) or tummy (ascites) from a build-up of fluid.
• loss of sex drive (libido)
Diagnosis

Tests
Your doctor may order one or more tests that may suggest a problem with your liver, including:

• Laboratory tests. Your doctor may order blood tests to check for signs of liver malfunction, such
as excess bilirubin, as well as for certain enzymes that may indicate liver damage. To assess kidney
function, your blood is checked for creatinine. You'll be screened for the hepatitis viruses. Your
international normalized ratio (INR) is also checked for your blood's ability to clot.

Based on the blood test results, your doctor may be able to diagnose the underlying cause of cirrhosis.
He or she can also use blood tests to help identify how serious your cirrhosis is.

• Imaging tests. Magnetic resonance elastography (MRE) may be recommended. This noninvasive
advanced imaging test detects hardening or stiffening of the liver. Other imaging tests, such as MRI,
CT and ultrasound, may also be done.

• Biopsy. A tissue sample (biopsy) is not necessarily needed for diagnosis. However, your doctor may
use it to identify the severity, extent and cause of liver damage.

If you have cirrhosis, your doctor is likely to recommend regular diagnostic tests to monitor for signs of disease
progression or complications, especially esophageal varices and liver cancer. Noninvasive tests are becoming more
widely available for monitoring.
• Abdominal computed tomography (CT) scan: This procedure combines special x-ray
equipment with sophisticated computers to produce multiple, digital images or pictures of the liver. It can
help determine the severity of cirrhosis as well as other liver diseases. See "Radiation Dose in X-Ray and
CT Exams"
• Abdominal ultrasound: Ultrasound is a type of imaging exam that uses sound waves to create pictures
of the inside of the abdomen and/or pelvis, including images of the liver. Doppler ultrasound allows for
evaluation of blood flow to and from the liver.
• Elastography: This exam assesses the stiffness of your liver and can help diagnose how severe the scarring
is in your liver (known as liver fibrosis). Left untreated, liver fibrosis can eventually lead to cirrhosis of the
liver which is not reversible. Elastography can detect stiffness of the liver caused by liver fibrosis earlier
than other imaging tests. The test can be performed by ultrasound or MRI.
• Body magnetic resonance imaging (MRI): This imaging exam uses a powerful magnetic field,
radio frequency pulses and a computer to produce detailed pictures of the liver allowing for assessment of
damage caused by various liver diseases. See the MRI Safety page for more information.
• Magnetic resonance cholangiopancreatography (MRCP) : MRCP is special type of MRI
protocol that is designed to evaluate a part of the liver and gallbladder, known as the biliary system that is
part of your liver.
Medication and doses
 DEPARTMENT OF
PHARMACY
PRACTICE
PATIENT PROFORMA

Patient Name: XYZ Age:45 YRS Gender: MALE Provisional Diagnosis:

• COPD
IP No.:0407 DOA:20/02/22 Height: 5.7 BMI: 28 • PORTALVEINHY
PERTENSION
DOD: 2/02/22 Weight: 72Kgs Department: • HEPATIC
GASTROENTEROLOGY HYDROTHORX

Reasons for admission: shortness of breath x15 days

• cough and expectoration with white sputum production
• orthopenia
• increased abdominal pain
• decreased urine output over past 5 days
• burning micturation
• no c/o haematemesis, no c/o altered sleep pattern
• no c/o fever, loss of appetite, weight loss

Past Medical History: NO/DM, HTN, Thyroid illness

Past Medication History: NA

Family History: nil

Social History:
Chronic alcoholic

Allergies: NA
DAY NOTES:

DAY1 DAY 2 DAY 3

Bp-100/70mmHg Bp- 130/50 mm hg Bp-110/70 mm hg
• Sp0 2-90% • PR-11/min • Sp02-88%
p/a- soft, • Spo2-+ve • P/asoft,
tenderness
• p/a-soft, mildtenderess,
• Fever-ve hepatomeghaly +ve
hepatosplenomegaly
• Abdomen • Pleural fluid
pain-ve • Adv
analysis
• Sob-ve • Pleural fluid
• c/o FUNGAL
analysis
• Stool – 1 KDH CBNAAT,
time • Pt/INR LDH
• USIE • Cytology, cell
• CECT CHEST count
fever - -ve • Repeat chest Xray
Abdomen pain-ve • PT
Stool-2 times • INR
• Collect CBP
Urine output-adequate Report

DAY 4 DAY 5 DAY 6

Bp -116/70mmhg
• Stool -
4 times
• Fever - Bp- 110/70mmhg Bp- 110/70 mm hg
ve • Stool- 3 times • Spo2-94%
• Sob -ve
• Pain
abdomen -
ve
• p/a -
soft
Nontenderness
heoatosolenomeghy
 DAY 7 DAY 8 DAY 9

Bp-110/70 mmhg
Bp-110/70 mmhg Bp- 100/70 mmhg • Spo 2-95%
• Spo 2-94% • Spo 2-94% • p/a -Soft,
Nontenderness
• Hepatosplenomeghaly
• Fever -ve
• Sob -ve
• Stool-2times
c/o no fresh complaints,
adv;the patient was adviced to
be discharged
OBJECTIVE- LAB INVESTIGATIONS
HAEMTOLOGY 01 02 03 04 05 ELECTROLYTES 01 02 03 04 05

Hb (11-16.5g. dl) Sodium

9.2 gm (135-
145mEq/l) 136mEq/L
PCV (35-50%) Potassium (3.5-
17.2 5.5mEq/l) 3.7mEq/L

TC (3500-10000/cum) Chlorides (98-

107mEq/l) 104mEq/l

DC Magnesium (1.6-
2.8mg/dl)
Lymphocytes (15- 0.78%
30%)
0.33% [Link](8.4-
Mid cells (2-10%) 10.8mg/dl) 8.61mg/dl

2.27%
Neutrophils (40-70%)

Eosinophils (1-6%) 0.96%

ESR:M(0-10mm/hr) 120 mm LIPID PROFILE 01 02 03 04 05

F(0-20mm/hr)

Platelets(1- Tot. Chol

4lac (130-
cells/cum) [Link])
RBC (3.80-5.80m/cu) 2.9/cmm HDL (30-70mg/dl)

Retic count (0.5-2.6%) T.G(upto170mg/dl)

BT VLDL(5-40mg/dl)

CT LDL (60-170mg/dl)

INR URINE ANALYSIS 01 02 03 04 05

PT Protein

APTT Sugar
-ve
LIVER FUNCTION 01 02 03 04 05 Pus cells
4-6
TEST Epi. cells
2-3
Total proteins
(6.8-8.3g/dl) 6.7
RBC’s
Albumin
2.9
THYROID
FUNCTION TEST
Globulin 3.8

A/G
1.3
TSH (0.4- 4.5U/mL)

Total T3 (80-220
ng/dL)
 Total T4 (5.0-
12.0μg/dL)
AST
59.5IU/L
ALT FT3 (260-
29.1IU/L 480pg/mL)

FT4(0.7-1.53
ng/dL)

ALP (36-142mu/l) RENAL 01 02 03 04 05

2.31U/L FUNCTION TEST

Bilirubin Total [Link]

(0.5-1.1mg/dl) 7.3mg/dl
M(0.6-1.1mg/dl)

Bilirubin F(0.5-0.9mg/dl)
Direct(upto3mg/dl) 2.8mg/dl

Bilirubin [Link](3-8mmol/l)
Indirect 4.5 mg/dl
(mg/dl)
GGTP
59 U/L
[Link] nitrogen
17.34mg
BLOOD (10- 50mg/dl)
GLUCOSE
/dl
Uric acid

FBS (70-110mg/dl) (2.6-7.2mg/dl)

RBS (110-180mg/dl) Urine Input/Output

PPBS (110-
160mg/dl)

Other Investigations:
Chest x ray view.
USG OF ABDOMIN
Impression: cirrhosis of liver with portal hypertension as evidenced by splenomegaly and gross tense
ascites
Cholelithiasis
Ascitic fluid examination
Right lung complete opacification seen.
Left side fields grossly clear.
Cardia grossly clear.
Bony thorax normal.

FINAL DIAGNOSIS:

Cirrhosis of the liver

MEDICATION CHART

Medication
S. Dose ROA Freq Indication Duration
No
Brand name Generic name 1 2 3 4 5 6

Infections of ✓ ✓ ✓ ✓ ✓ ✓
1 Inj. Monocef Ceftriaxone 1mg IV BD lower
respiratory tract
Treatment of ✓ ✓ ✓ ✓ ✓ ✓
2 Tab. Lasix resistant oedema
Lasilactone 20/80m PO OD
g
Hypertension , ✓ ✓ ✓ ✓ ✓ ✓
3 Tab Ciplar Propranolol(Ind 40 mg PO HS Angina,
eral) Arrhythmia
HBV in adults ✓ ✓ ✓ ✓ ✓ ✓
4 Tab. 25mg
Tenofovir Emtricitabine- IV OD
alfanamide tenofovir

Acne , ✓ ✓ ✓ ✓ ✓ ✓
5 Thiamine (vit 1 Amp IV OD Allergies,
[Link] B1) Alzheimer
disease
Diarrhea , IBD ✓ ✓ ✓ ✓ ✓ ✓
6 Tab. Rifagut Rifaximin IV BD
550mg

DISCHARGE MEDICATION & ADVICE:

ADR: Intervention: Drug Information: Patient counselling:

Student name and signature with date: Name and signature of preceptor with date:
 SOAP NOTES

SUBJECTIVE:

➢ A 45 yrs old male patient was presented with complaints of severe radiating abdominal pain
&diarrhea was admitted for further evaluation management

➢ Patient is a known case of liver cirrhosis

OBJECTIVE:

LFT:

• Bilirubin T – 7.3 mg/dl

• Bilirubin D -2.8 mg/dl
• AST: 59.5 U/L
• ALT: 29.1 U/L
• ALP; 2.31 U/L

BIOCHEMISTRY
• B. Urea: 17.34 mg/dl
• [Link] 0.7 mg/dl

ASSESSMENT:

➢ Based on subjective evidence i.e; chief complaints and objective evidences the patient was diagnosed
confirmed as Cirrhosis of the li
PLANNING:

Goals of treatment:

➢ The main goal of treatment is to prevent progression of disease .

➢ The best way to do this is to diagnose the disease early and control the underlying cause.
➢ Reduce signs and symptoms.
➢ Improve health condition of patient.
➢ To avoid disease related complications.

MEDICATION:

1. MONOCEF:( Ceftriaxone)
Dose: 1gm
ROA; IV
MOA:
works by inhibiting the mucopeptide synthesis in the bacterial cell wall. The beta-lactam moiety of
ceftriaxone binds to carboxypeptidases, endopeptidases, and transpeptidases in the bacterial cytoplasmic
membrane. These enzymes are involved in cell-wall synthesis and cell division.
INDICATION:
Treatment of infections of lower respiratory tract, urinary tract, skin and skin structures, bone and joint; treatment
of intra-abdominal infections, pelvic inflammatory disease, gonorrhea, septicemia and meningitis due to
susceptible microorganisms.
Side effects:
• Skin rash
• Diarrhoea
• nausea
2. LASILACTONE:
Dose: 20/80mg
ROA: PO
MOA:
Lasilactone contains a short-acting diuretic and a long-acting aldosterone antagonist. It is indicated in the
treatment of resistant oedema where this is associated with secondary hyperaldosteronism; conditions include
chronic congestive cardiac failure and hepatic cirrhosis.
 INDICATION:
It is indicated in the treatment of resistant oedema where this is associated with secondary
hyperaldosteronism; conditions include chronic congestive cardiac failure and hepatic cirrhosis.
Side effects:
• Dehydration
• Hyponatremia
• Increased blood cholesterol
3. CIPLAR(PropranololInderal))
Dose: 40 mg
ROA: PO
MOA:
Blocks the effect of some chemicals on your heart and blood vessels. This slows down the heart rate and helps
the heartbeat with less force thereby lowering your blood pressure. It is used for the immediate reduction of very
high blood pressure (hypertensive emergency).
INDICATION:
Ciplar-10 Tablet 15's belongs to a group of medicines called beta-blockers used alone or together with other
medicines to treat high blood pressure (hypertension), heart-related chest pain (angina), heart rhythm
disorder (arrhythmia) and preventing symptoms of migraine headache and tremors (fits).

Side effects:
• Slow heart beat
• Nausea
• Vomiting

4. TENOFOVIR ALFANAMIDE

Dose: 25 mg
ROA: IV
MOA:
Tenofovir alafenamide has been shown to be a potent inhibitor of hepatitis B viral replication. Tenofovir
alafenamide presents a better renal tolerance when compared with the counterpart tenofovir disoproxil. This
improved safety profile seems to be related to a lower plasma concentration of tenofovir.
INDICATON:
Tenofovir alafenamide is an antiviral prescription medicine approved by the U.S. Food and Drug Administration
(FDA) for the treatment of hepatitis B virus infection (HBV) in adults who meet certain requirements.
 Side effects:
• Abdominal discomfort
• Bloody urine
• Decreased appetite
• Increased blood pressure

5. OPTINEURON
Dose: 1 Amp
ROA: IV
Optineuron Injection is a nutritional supplement and helps to improve the level of vitamin B12 in your body.
Vitamin B12 is essential in the formation of red blood cells and helps in absorption of iron in the body. As a result
of this your haemoglobin level increases.
INDICATIO
Optineuron Injection is a Injection manufactured by LUPIN LABS. It is commonly used for the diagnosis or
treatment of acne, allergies, alzheimer's disease .
Side effects:
• Diarrhea
• Tiredness
• Nausea
• Sleepiness

6. RIFAGUT
Dose: 550 mg
ROA: IV
MOA
Rifaximin is a poorly absorbed bactericidal rifamycin derivative, which inhibits bacterial protein synthesis by
irreversibly binding to RpoB, the beta-subunit of the bacterial DNA-dependent RNA polymerase
INDICATION :
Rifagut 400 Tablet is also used to treat infectious diarrhea and irritable bowel syndrome with diarrhea (IBS-
D) in adults and children.
Side effects:
• Headache
• Peripheral oedema
• Nausea
• Fatigue
Goals achieved
• Sign and symptoms are reduced
• Patient health condition improved
• Decreased liver cirrhosis

Monitoring parameters

▪ RBC levels
▪ CBC
▪ LFT
▪ ESR levels
▪ SGOT levels
▪ SGPT levels
▪ ALP levels
▪ BUN levels

Problems identified

NO

PATIENT COUNSELLING:
About The Disease:

➢ Patient was clearly explained regarding his disease condition and its further complications
About Medication:

➢ Patient was clearly explained about dose, route & freq of medication
➢ Also explained about medication adherence
➢ If any ADR is report to physician immediately
LIFESTYLE MODIFICATIONS

➢ Eat smaller and more frequent meals each day instead of a few large
meals. This promotesdigestion and can aid in preventing heartburn.
➢ Wear loose-fitting clothes to ease pressure on the stomach, which can
worsen heartburn andreflux.
➢ Quit smoking. Smoking can increase the production of stomach
acid and reduce the function of the lower esophageal sphincter, the
muscle that keeps acid and other stomachcontent from reentering
the esophagus. Smoking can also decrease the amount of saliva,
which neutralizes acid produced by the body. Experts at NYU
Langone’s Tobacco Cessation Programs can advise you on how to
quit smoking for good.
➢ Avoid lying down for at least two hours after a meal or after drinking
acidic beverages, likesoda, or other caffeinated beverages. This can
help to prevent stomach contents from flowing back into the
esophagus

FOOD TO BE TAKEN
➢ Pastas.

➢ Rice.
➢ Lean meats prepared with little fat.

➢ Low-fat cooked fish.

➢ Eggs.

➢ Fresh fruits, or fruits canned in their own juice.

➢ Cooked vegetables.

➢ Sugar-free cereals
FOOD TO AVOID

➢ Fruit juices that contain a lot of sugar and fruit drinks.

➢ Sports drinks such as Gatorade.

➢ Soft or carbonated drinks.

➢ Caffeinated drinks.

➢ Broths and canned or packaged soups.

➢ Fried foods or those rich in fat (delicatessen, potato chips, French fries, pastries)